Following spinal cord injury in human males, fertility is severely impaired. There are two major problems underlying this reduced infertility. The first is a profound impairment of ejaculation. The second is poor semen quality and volume. Our hypothesis is that these two problems may both be caused by disruption of seminal emission following spinal transection. We have shown that ejaculation is a stereotyped reflex elicited by the buildup of seminal fluids in the urethra. We hypothesize that the ejaculatory difficulties in spinal cord injured patients are due to seminal volumes which are inadequate to elicit ejaculation. Impairment of seminal emission may also be responsible for poor semen quality because secretions from the accessory sex glands are important for maintenance of an appropriate environment for sperm. The efferent innervation of the accessory sex glands is well known and the broad outlines of the pharmacology of this innervation have been elucidated. Both sympathetic and parasympathetic mechanisms are believed to be involved in mediating seminal emission. However, virtually nothing is known about the reflex regulation of this outflow. These studies will determine, for the first time, the properties of the reflexes mediating seminal emission in intact animals. Well established multiunit nerve recording techniques will be used to record sympathetic and parasympathetic pre- and postganglionic innervation of the accessory sex glands. Both electrical and physiological stimuli of pelvic afferents will be used to elicit emission reflexes. The functional consequences of the reflexes will be assessed by measuring seminal fluid secretory rate and composition. Our hypothesis is that the reflexes mediating seminal emission are suppressed following spinal transection. These experiments will test this hypothesis and determine if particular components of the reflexes are more affected by transection. In particular, pharmacological studies have demonstrated that seminal secretion is regulated by a synergistic control by sympathetic and parasympathetic mechanisms. Parasympathetic stimulation gives rise to a long lasting epithelial secretion, whereas sympathetic stimulation primarily causes fluid expulsion by smooth muscle contraction. It is important to know if both classes of reflexes are depressed following spinal cord transection. Immunohistochemical studies have shown that the autonomic efferent neurons innervating the pelvis receive extremely dense descending projections containing neuromodulatory substances such as serotonin and norepinephrine. A very dense innervation by opiates, both spinal and supraspinal, has also been described. In this series of experiments, we will test the effects of receptor-specific agonists and antagonists of these transmitters on emission reflexes in transected animals. The goal will be to identify effective and easily tolerated treatments to enhance seminal emission following spinal cord transection.